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Related Concept Videos

Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
Cellular Adaptation II: Hypertrophy01:26

Cellular Adaptation II: Hypertrophy

Hypertrophy is the increase in the size of individual cells, resulting in the enlargement of a tissue or organ. Unlike hyperplasia, which involves an increase in cell number, hypertrophy is characterized by an increase in cell volume. This process often occurs in response to higher functional demand or hormonal stimulation, leading to the production of more structural proteins and organelles, thereby enhancing the cells' work capacity.There are two primary types of hypertrophy: physiological...
Heart Failure Drugs: β-Blockers01:22

Heart Failure Drugs: β-Blockers

β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation, vasodilation, and...
Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...

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Related Experiment Video

Updated: Jun 17, 2026

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
09:16

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

Published on: June 3, 2018

TFEB Antagonizes Cardiac Hypertrophy and Failure by Enhancing Lysosomal Capacity and Mitochondrial Function.

Daniel Daou1,2, Subhajit Das Gupta1,2, Anip Anand1,2

  • 1Department of Internal Medicine (Cardiology) (D.D., S.D.G., A.A., H.I.M., N.J., C.I.I., A.F., V.G.-M., N.N., L.M.-R., D.D.Z., F.O.-S., G.C., F.W., B.A.R., L.I.S., S.L., T.G.G., J.A.H.), UT Southwestern Medical Center, Dallas, TX.

Circulation Research
|June 16, 2026
PubMed
Summary

Transcription factor EB (TFEB) protects against pathological cardiac remodeling by enhancing lysosomal function and mitochondrial energy production. Loss of TFEB exacerbates heart failure due to impaired protein turnover and signaling pathways.

Keywords:
autophagyheart failurehypertrophylysosomesproteomics

Related Experiment Videos

Last Updated: Jun 17, 2026

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
09:16

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

Published on: June 3, 2018

Area of Science:

  • Cardiovascular Biology
  • Cellular Metabolism
  • Molecular Cardiology

Background:

  • Pathological cardiac remodeling and increased energy demand contribute to heart failure (HF).
  • Lysosomal processes and mitochondrial function are crucial in cardiac remodeling and HF.
  • Transcription factor EB (TFEB) regulates lysosomal genes and mitochondrial function, particularly under stress.

Purpose of the Study:

  • To investigate the role of TFEB in cardiomyocyte hypertrophy and pressure overload-induced heart failure.
  • To elucidate the molecular mechanisms by which TFEB influences cardiac remodeling and function.

Main Methods:

  • Utilized a cardiomyocyte-specific TFEB knockout mouse (CTKO) model subjected to transverse aortic constriction (TAC).
  • Assessed cardiac function using echocardiography and performed transcriptomic, proteomic, and metabolomic analyses.
  • Employed neonatal rat ventricular myocytes treated with phenylephrine as an in vitro model of hypertrophy.

Main Results:

  • TFEB activation in cardiomyocytes triggers a lysosomal gene program under hypertrophic stress.
  • CTKO mice exhibited exacerbated hypertrophy and rapid heart failure following TAC, with impaired lysosomal capacity and protein turnover.
  • Loss of TFEB led to altered mitochondrial structure, reduced oxidative capacity, and impaired metabolic enzyme expression, alongside decreased AMP-activated protein kinase (AMPK) signaling.
  • In vitro and in vivo studies showed that TFEB activation has anti-hypertrophic effects and that exogenous AMPK activation can rescue the hypertrophic response.

Conclusions:

  • TFEB antagonizes pathological cardiac remodeling by upregulating lysosomal capacity and maintaining mitochondrial function.
  • TFEB plays a critical role in promoting AMPK signaling, which is essential for managing hypertrophic stress.
  • These findings highlight TFEB as a key regulator of cardiac adaptation to stress and a potential therapeutic target for heart failure.